Wu S G, Jeng F R, Wei S Y, Su C Z, Chung T C, Chang W J, Chang H W
Department of Internal Medicine, Municipal General Hospital for Women and Children, Kaohsiung, Taiwan, Republic of China.
Nephron. 1998;78(1):28-32. doi: 10.1159/000044878.
Chronic renal failure induces anemia and a short erythrocyte life span. Red blood cell (RBC) osmotic fragility is the resistance of RBC hemolysis to osmotic changes that is used to evaluate RBC friability. To find the cause of shortened red cell survival in uremic patients, we evaluated the RBC osmotic fragility in 57 chronic hemodialyzed patients. Each patient had received 12 h of dialysis per week continuously prior to being enrolled in the study. Nineteen healthy volunteers served as a control group. Biochemistry, hemoglobin, electrolyte, osmolarity, beta2-microglobulin, and intact parathyroid hormone were examined before and after the dialysis session. To evaluate the osmotic fragility of RBC, blood samples were collected in heparinized test tubes. Fifty microliters of the RBC of each individual was then incubated in solutions containing a series of various concentrations of NaCl ranging from 0 to 0.6%. The concentration of NaCl at which 50% of RBCs were lysed was considered the median osmotic fragility (MOF). The results showed that the MOF was significantly greater in hemodialyzed patients before dialysis than in the control group (0.41 +/- 0.03 vs. 0.39 +/- 0.02%). The osmotic resistance to hemolysis was also recorded after dialysis (MOF 0.38 +/- 0.03%). Correlation analysis showed that the MOF was significantly correlated with urea nitrogen, serum osmolarity, and intact parathyroid hormone level. In addition, the osmotic fragility was higher in patients who had a predialysis intact parathyroid hormone level > 100 pg/dl. In conclusion, hemodialysis can improve the osmotic fragility. The mechanism underlying this improvement may be the removal of low molecular weight uremic toxins, resulting in normalization of serum osmolarity. Our results indicate that parathyroid hormone is probably a major factor influencing RBC osmotic fragility in chronic renal failure.
慢性肾衰竭会引发贫血以及红细胞寿命缩短。红细胞渗透脆性是指红细胞对渗透变化的溶血抵抗力，用于评估红细胞的脆性。为了找出尿毒症患者红细胞存活期缩短的原因，我们评估了57例慢性血液透析患者的红细胞渗透脆性。在纳入本研究之前，每位患者每周连续接受12小时的透析治疗。19名健康志愿者作为对照组。在透析前后检测生化指标、血红蛋白、电解质、渗透压、β2-微球蛋白和完整甲状旁腺激素。为了评估红细胞的渗透脆性，将血样采集到肝素化试管中。然后将每个个体的50微升红细胞在含有一系列不同浓度（0至0.6%）氯化钠的溶液中孵育。50%红细胞发生溶血时的氯化钠浓度被视为中位数渗透脆性（MOF）。结果显示，透析前血液透析患者的MOF显著高于对照组（0.41±0.03对0.39±0.02%）。透析后也记录了对溶血的渗透抵抗力（MOF为0.38±0.03%）。相关性分析表明，MOF与尿素氮、血清渗透压和完整甲状旁腺激素水平显著相关。此外，透析前完整甲状旁腺激素水平>100 pg/dl的患者，其渗透脆性更高。总之，血液透析可改善渗透脆性。这种改善的潜在机制可能是清除了低分子量尿毒症毒素，从而使血清渗透压恢复正常。我们的结果表明，甲状旁腺激素可能是影响慢性肾衰竭患者红细胞渗透脆性的主要因素。
